miR-203a regulates proliferation, migration, and apoptosis by targeting glycogen synthase kinase-3β in human renal cell carcinoma
miR-203a regulates proliferation, migration, and apoptosis by targeting glycogen synthase kinase-3β in human renal cell carcinoma
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DOI：
10.1007/s13277-014-2476-x
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发表时间：
2014-11-01
期刊：
影响因子：
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通讯作者：
Xu, Yunfei
中科院分区：
文献类型：
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作者：
Hu, Guanghui;Lai, Peng;Xu, Yunfei
microRNA在癌症进展和转移中起着至关重要的作用。miR-203 a已被鉴定为多种癌症中的肿瘤抑制因子。然而，其在肾细胞癌中的功能尚未阐明。本研究检测miR-203 a在肾癌组织中的表达，并探讨其与肾癌临床特征的关系。肾癌组织和肾癌细胞中存在miR-203 a的过表达。miR-203 a高表达与肿瘤分期和总生存时间短相关。生物信息学和荧光素酶检测证实糖原合成酶激酶-3 β是miR-203 a的靶基因。miR-203 a基因沉默可抑制细胞增殖和迁移，使其阻滞于G1期，促进细胞凋亡。miR-203 a促进肾细胞癌的进展并预测不良预后。
MicroRNAs play a crucial role in cancer progression and metastasis. miR-203a has been identified as a tumor suppressor in various cancers. However, its functions in renal cell carcinoma have not been illustrated. In this study, we detected the miR-203a expression in renal cell carcinoma and evaluated its association with clinical features. Overexpression of miR-203a was found in renal cell carcinoma tissues and renal cell carcinoma cells. High miR-203a expression is correlated with tumor stage and short overall survival time. Bioinformatics and luciferase assay confirmed that glycogen synthase kinase-3 beta was a target gene of miR-203a. Silencing of miR-203a could inhibit cell proliferation and migration, arrest them in G1 phase, and promote apoptosis in vitro. miR-203a promotes the progression of renal cell carcinoma and predicts a poor prognosis.